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1 he Nogo-66 receptor-1 (NgR1) and its homolog NgR2.
2 outgrowth but fail to associate with NgR1 or NgR2.
3 -66, and MAG compared with wild-type NgR1 or NgR2.
4 expression of a GPI-linked surface molecule, NgR2, also known as Nogo-66 receptor homolog 1.
5 son of NgR surface residues not conserved in NgR2 and NgR3, identifies potential protein interaction
6 e similarity with NgR, two related proteins, NgR2 and NgR3, which we have identified, do not bind Nog
7                        Nogo receptors (NgR1, NgR2, and NgR3) are growth cone directive molecules know
8 receptors of the Nogo Receptor family (NgR1, NgR2, and NgR3) restrict excitatory synapse formation.
9  of the structurally related molecules NgR1, NgR2, and NgR3.
10 levels of alphaVbeta3 and, as shown here, of NgR2 are detected in human and mouse NEPrCa, our finding
11                  In postnatal brain NgR1 and NgR2 are strongly enriched in Triton X-100-insoluble lip
12    The Nogo receptor family members NgR1 and NgR2 bind to MAIs and have been implicated in neuronal i
13        The CT-cap domain and stalk region of NgR2, but not NgR1, are sufficient for MAG binding, and
14     We also confirmed here that MAG binds to NgR2, but not to NgR3.
15                                    MAG binds NgR2 directly and with greater affinity than NgR1.
16                                      Soluble NgR2 has MAG antagonistic capacity and promotes neuronal
17        Neural expression studies of NgR1 and NgR2 have revealed broad and overlapping, yet distinct,
18 e first evidence for a physiological role of NgR2 in the peripheral nervous system.
19                            Here we show that NgR2 is a novel receptor for MAG and acts selectively to
20 nt with its role as a neuronal MAG receptor, NgR2 is an axonassociated glycoprotein.
21 e we report that the Nogo66 receptor homolog NgR2 is essential for proper cutaneous innervation.
22                         Forced expression of NgR2 is sufficient to impart MAG inhibition to neonatal
23                            We show here that NgR2 is upregulated by alphaVbeta3, to which it associat
24    Structural studies have revealed that the NgR2 leucine-rich repeat cluster and the NgR2 "unique" d
25                                              NgR2(-/-) mice display increased density of nonpeptiderg
26 f total measured area in APP(swe)/PS1DeltaE9/NgR2(-/-) mice vs. 0.76% of total measured area in APP(s
27 gr3 (Ngr1(-/-); Ngr3(-/-)), but not Ngr1 and Ngr2 (Ngr1(-/-); Ngr2(-/-)), was sufficient to mimic the
28     Nogo receptor triple mutants (Ngr1(-/-); Ngr2(-/-); Ngr3(-/-); which are also known as Rtn4r, Rtn
29 ly and with high affinity to NgR1 but not to NgR2 or NgR3.
30                         However, deletion of NgR2 renders nociceptive nonpeptidergic sensory neurons
31                  This study is novel because NgR2 role has only minimally been investigated in cancer
32               The data suggest that Versican/NgR2 signaling at the dermo-epidermal junction acts in v
33              Biochemical evidence shows that NgR2 specifically interacts with the G3 domain of Versic
34 followed by a 13 aa MAG-binding motif of the NgR2 stalk, shows superior binding of OMgp, Nogo-66, and
35                          In neurons NgR1 and NgR2 support MAG binding in a sialic acid-dependent Vibr
36 the NgR2 leucine-rich repeat cluster and the NgR2 "unique" domain are necessary for high-affinity MAG
37                                         When NgR2 was ablated in AD transgenic mice expressing Swedis
38 gr3(-/-)), but not Ngr1 and Ngr2 (Ngr1(-/-); Ngr2(-/-)), was sufficient to mimic the triple mutant re